Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1061584 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27468982.fastq.gz | Fastqsanger.gz | |||
| SRR27468983.fastq.gz | Fastqsanger.gz | |||
| SRR27468984.fastq.gz | Fastqsanger.gz | |||
| SRR27468985.fastq.gz | Fastqsanger.gz | |||
| SRR27468986.fastq.gz | Fastqsanger.gz |
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Project description:Exploring molecular details of carbon utilization trade-offs in galactose-evolved yeast Adaptively evolved yeast mutants on galactose for around 400 generations showed diminished growth and carbon uptake rates on glucose. Genome-scale approaches were applied to characterize the molecular genetic basis of these trade-offs in carbon source utilization. Engineered mutants showing trade-offs in a specific carbon uptake rate between both carbons were used as controls. The transcriptional responses of the evolved mutants were almost identical during growth on both carbon sources. These carbon-independent conserved patterns were clearly observed in specific pathways and genes. Up-regulation of PGM2, a confirmed beneficial genetic change for improving galactose utilization was preserved on both carbons. In addition, HXK1, GLK1 and genes involved in reserve carbohydrate metabolism were up-regulated, while HXK2 was down-regulated. Genes that have a transcription factor binding site for Gis1p, Rph1p, Msn2/4p and Nrg1p were up-regulated. These results indicated changes in the metabolic pathways involved in metabolism of both carbons and in nutrient signaling pathway. The concentration profile of trehalose and glycogen supported these findings. Mutations in RAS2 and ERG5 genes were selected because of their beneficial and neutral effect on galactose utilization, respectively in our previous study. Site-directed mutants containing galactose-beneficial mutations in RAS2 only resulted in a significant decrease in glucose utilization. Integration of all these analyses clearly suggest an antagonistic pleiotropic trade-off in carbon source utilization caused by changes in regulatory region, and we hereby demonstrate how systems biology can be used to gain insight into evolutionary processes at the molecular level. Yeast galactose evolved mutants having improved galactose availability were grown on aerobic batch with glucose as carbon source
2012-07-31 | E-GEOD-39065 | biostudies-arrayexpress
Project description:Exploring molecular details of carbon utilization trade-offs in galactose-evolved yeast Adaptively evolved yeast mutants on galactose for around 400 generations showed diminished growth and carbon uptake rates on glucose. Genome-scale approaches were applied to characterize the molecular genetic basis of these trade-offs in carbon source utilization. Engineered mutants showing trade-offs in a specific carbon uptake rate between both carbons were used as controls. The transcriptional responses of the evolved mutants were almost identical during growth on both carbon sources. These carbon-independent conserved patterns were clearly observed in specific pathways and genes. Up-regulation of PGM2, a confirmed beneficial genetic change for improving galactose utilization was preserved on both carbons. In addition, HXK1, GLK1 and genes involved in reserve carbohydrate metabolism were up-regulated, while HXK2 was down-regulated. Genes that have a transcription factor binding site for Gis1p, Rph1p, Msn2/4p and Nrg1p were up-regulated. These results indicated changes in the metabolic pathways involved in metabolism of both carbons and in nutrient signaling pathway. The concentration profile of trehalose and glycogen supported these findings. Mutations in RAS2 and ERG5 genes were selected because of their beneficial and neutral effect on galactose utilization, respectively in our previous study. Site-directed mutants containing galactose-beneficial mutations in RAS2 only resulted in a significant decrease in glucose utilization. Integration of all these analyses clearly suggest an antagonistic pleiotropic trade-off in carbon source utilization caused by changes in regulatory region, and we hereby demonstrate how systems biology can be used to gain insight into evolutionary processes at the molecular level.
2012-08-01 | GSE39065 | GEO
Project description:Legumes establish nitrogen-fixing symbiosis with beneficial rhizobia. On the other hand, they might be attacked concomitantly by pathogens raising the question of potential trade-off between mutualism and immunity. Here, using a tripartite system involving the model legume Lotus japonicus, its rhizobial symbiont Mesorhizobium loti and the soil-borne pathogen Ralstonia solanacearum we investigated such trade-offs. We found that interaction with M. loti increases plant resistance against the pathogen without impairing mutualism. Genetic and proteomics characterisation indicate that Lotus resistance is mediated by Effector Triggered Immunity and is associated with distinct proteome modifications in roots and nodules. The inoculation of rhizobia, even if they are not mutualist, increases plant resistance. Our results question the concept of interference between efficient defense reactions and mutualistic interactions and is of great interest for agricultural purposes as it not only restricts pathogen colonisation but would also preserve nitrogen fixation and yield.
2024-01-30 | PXD048803 | Pride
Project description:Cell growth rate is regulated in response to resource availability including the abundance, and molecular form, of essential nutrients. In the model eukaryotic cell, Saccharomyces cerevisiae (budding yeast), the molecular form of environmental nitrogen impacts both cell growth rate and mRNA expression. Disentangling causal relationships between nitrogen availability, cell growth rate and differential gene expression poses a considerable challenge. Using experimental control of cell growth rate using chemostats, we studied the effect of variation in environmental nitrogen on differential gene expression. We find that the primary determinant of nitrogen-regulated gene expression is nitrogen abundance whereas variation in nitrogen source affects the expression of only a small number of transcripts with highly specialized functions. To study the dynamics of nitrogen-responsive gene expression we perturbed steady-state nitrogen-limited chemostat cultures by addition of either proline or glutamine. Addition of either proline or glutamine to cells growing in nitrogen-limited chemostats results in repression of the nitrogen catabolite repression (NCR) regulon consistent with nitrogen abundance, and not nitrogen source, being the primary determinant of nitrogen-regulated gene expression. We find that a transition from nitrogen-limited to nitrogen-replete conditions is accompanied by rapid induction of transcripts required for protein translation. We identified a reciprocal relationship between specific regulons required for protein translation (RP and RiBi) and the NCR regulon. Using mathematical modeling we find evidence that cells adopt a metabolically inefficient growth mode during this transition. By means of high resolution time series analysis we find evidence that rapid, and potentially accelerated, mRNA degradation plays an important role in remodeling gene expression programs in response to change in environmental nitrogen. We propose that the evolutionarily conserved TORC1 signaling pathway orchestrates the balance between protein translation and assimilation of nitrogen sources at the transcriptional level to optimize rates of cell proliferation.
2014-05-05 | GSE57293 | GEO
Project description:The impacts of man-made chemicals, in particular of persistent organic pollutants, are multifactorial as they may affect the integrity of ecosystems, alter biodiversity and hinder the health of most organisms. We have demonstrated that the belowground mycobiota of forest soils acts as a buffer against the pollution provoked by the biocide pentachlorophenol. However the trade-offs of the mitigation of the pollutant remain cryptic. To address this question we scrutinised the key changing aspects of a metacommunity of fungi when confronted (or not) with the biocide, comprising taxonomic and functional levels, as well as the identification of the major pollutant degraders within the metacommunity. Exposure to the biocide led to alterations in the metacommunity composition and functioning, many of which were not fully alleviated when most of the biocide was degraded, especially the dysregulation of the carbon and nitrogen metabolisms. The last is possibly linked to the higher pathogenic potential of the metacommunity after exposure to the biocide, supported by the secretion of proteins related to pathogenicity and reduced susceptibility to a standard fungicide. Our findings provide additional evidence for the silent risks of environmental pollution, particularly as it may favour the development of pathogenic trade-offs in fungi, which may impose serious threats to animals and plant hosts.
2018-11-28 | PXD009798 | Pride
Project description:The transcriptome and DGE analysis of the fat body and ovary of L. migratoria based on the Illumina short-read sequencing technology and De novo assembly. Research on the trade-offs between immunity and reproduction is contributing significantly to the understanding of the fitness of organisms in nature.
2017-05-01 | GSE57437 | GEO
Project description:Background: Variation in locomotor capacity among animals often reflects adaptations to different environments. Despite evidence that physical performance is heritable, the molecular basis of locomotor performance and performance trade-offs remains poorly understood. In this study we identify the genes, signaling pathways, and regulatory processes responsible for the trade-off between burst performance and endurance observed in Xenopus allofraseri, using a transcriptomic approach. Results: We obtained a total of about 121 million paired-end reads from Illumina RNA sequencing and analyzed 218,541 transcripts obtained from a de novo assembly. We identified 109 transcripts with a significant differential expression between endurant and burst performant individuals (FDR ≤ 0.05 and logFC ≥ 2), and blast searches resulted in 103 protein-coding genes. We found major differences between endurant and burst-performant individuals in the expression of genes involved in the polymerization of actin filaments, cellular trafficking, proteoglycans and extracellular proteins secreted, lipid metabolism, mitochondrial activity and regulators of signaling cascade. Remarkably, we revealed transcripts isoforms of key genes with function in metabolism, apoptosis, nuclear export and as transcriptional corepressor, expressed in either burst-performant or endurant individuals. Lastly, we find two up-regulated transcripts in burst-performant individuals that correspond to the expression of myosin-binding protein C fast-type (mybpc2). This suggests the presence of mybpc2 homoeologs and may have been favored by selection to permit fast and powerful locomotion. Conclusion: Locomotor performance trade-off in Xenopus allofraseri can be attributed to the differential expression of genes belonging to the different pathways of calcium signaling, endoplasmic reticulum stress response and striated muscle contraction, but also attributed to the use of alternative splicing and regulatory processes. Ultimately, our transcriptomic analysis offers new perspectives for future analyses of the role of single nucleotide variants, homoeology and alternative splicing in the evolution of locomotor performance trade-offs.
2021-01-31 | GSE157915 | GEO
Project description:Changes in the rate and fidelity of mitochondrial protein synthesis impact the metabolic and physiological roles of mitochondria. Here we explored how environmental stress in the form of a high-fat diet modulates mitochondrial translation using mutant mice with error-prone (Mrps12ep/ep) or hyper-accurate (Mrps12ha/ha) mitochondrial ribosomes. Intriguingly, although both mutations are metabolically beneficial in reducing body weight, decreasing circulating insulin and increasing glucose tolerance during a high-fat diet, they manifest divergent (either deleterious or beneficial) outcomes in a tissue-specific manner. In two distinct organ types that are commonly affected by metabolic disease, the heart and the liver, Mrps12ep/ep mice were protected against heart defects but sensitive towards lipid accumulation in the liver, activating genes involved in steroid and amino acid metabolism. In contrast, enhanced translational accuracy in Mrps12ha/ha mice protected the liver from a high-fat diet through activation of liver proliferation programs, but enhanced the development of severe hypertrophic cardiomyopathy. While these findings reflect the complex transcriptional and cell signalling responses that differ between post-mitotic (heart) and highly proliferative (liver) tissues, they also suggest that trade-offs between the rate and fidelity of mitochondrial protein synthesis dictate tissue-specific outcomes toward commonly encountered stressful environmental conditions.
2021-06-22 | GSE159014 | GEO